Levels Of Dietary Sodium Intake Research Articles

Sodium Intake and Atopic Dermatitis

The association of diet with atopic dermatitis (AD) remains poorly understood and could help explain heterogeneity in disease course. To determine the extent to which a higher level of dietary sodium intake, estimated using urine sodium as a biomarker, is associated with AD in a large, population-based cohort. This cross-sectional study of adult participants (aged 37-73 years) from the UK Biobank examined 24-hour urine sodium excretion, which was estimated using a single spot urine sample collected between March 31, 2006, and October 1, 2010, and calculations from the sex-specific International Cooperative Study on Salt, Other Factors, and Blood Pressure equation, incorporating body mass index; age; and urine concentrations of potassium, sodium, and creatinine. The data were analyzed between February 23, 2022, and March 20, 2024. The primary exposure was 24-hour urinary sodium excretion. The primary outcome was AD or active AD based on diagnostic and prescription codes from linked electronic medical records. Multivariable logistic regression models adjusted for age, sex, race and ethnicity, Townsend Deprivation Index, and education were used to measure the association. The analytic sample comprised 215 832 participants (mean [SD] age, 56.52 [8.06] years; 54.3% female). Mean (SD) estimated 24-hour urine sodium excretion was 3.01 (0.82) g per day, and 10 839 participants (5.0%) had a diagnosis of AD. Multivariable logistic regression revealed that a 1-g increase in estimated 24-hour urine sodium excretion was associated with increased odds of AD (adjusted odds ratio [AOR], 1.11; 95% CI, 1.07-1.14), increased odds of active AD (AOR, 1.16; 95% CI, 1.05-1.28), and increased odds of increasing severity of AD (AOR, 1.11; 95% CI, 1.07-1.15). In a validation cohort of 13 014 participants from the National Health and Nutrition Examination Survey, a 1 g per day higher dietary sodium intake estimated using dietary recall questionnaires was associated with a higher risk of current AD (AOR, 1.22; 95% CI, 1.01-1.47). These findings suggest that restriction of dietary sodium intake may be a cost-effective and low-risk intervention for AD.

DOSE-RESPONSE EFFECT OF SODIUM REDUCTION ON BLOOD PRSSURE IN TREATED HYPERTENSIVES: A SYSTEMATIC REVIEW AND INSTRUMENTAL VARIABLE META-ANALYSIS

Objective: To evaluate the dose-response effects of a reduction in dietary sodium intake on blood pressure (BP) in hypertensive individuals who were on antihypertensive treatments. The impact of antihypertensive-drug class was also examined. Design and method: We searched Medline (via Ovid), Embase, Scopus, Cochrane Central Register of Controlled Trials, and reference lists of relevant articles up to 12 November 2023. We included randomised controlled trials (RCTs) comparing the effect on BP between different levels of dietary sodium intake in adults who were diagnosed as primary hypertension and treated with constant antihypertensive medications during the study period. We excluded RCTs with duration < 2 weeks. Dietary sodium intake was measured using 24-hour urinary sodium excretion. Instrumental variable meta-analyses were conducted to evaluate the dose-response effects of sodium reduction on BP. Subgroup analysis and multivariate meta-regression analysis were performed to examine the impact of antihypertensive-drug class. Results: 35 studies with 2885 participants were included. The pooled estimates of mean reduction in 24-hour urinary sodium excretion, systolic BP (SBP), diastolic BP (DBP), and mean arterial pressure (MAP) were 68.74 (95% confidence interval: 62.30-75.19) mmol, 4.33 (3.37-5.29) mmHg, 2.60 mm Hg (2.04-3.17), and 3.19 (2.50-3.87), respectively. For every 100 mmol reduction in 24-hour urinary sodium excretion, SBP, DBP, and MAP decreased by 6.81 (4.96-8.66) mmHg, 3.85 (2.26-5.43) mmHg, and 4.83 (3.22-6.44) mmHg, respectively (Fig 1). The observed dose-response effects differed across class of antihypertensive medication (P-diff = 0.084 for SBP, and P-diff<0.05 for DBP and MAP). In Beta-blockers, Renin-Angiotensin-Aldosterone System (RAAS) inhibitors, and dual therapy groups, significant dose-response effects of sodium on SBP, DBP and MAP were observed. In Calcium Chanel Blockers (CCB) group, the dose-response relationship was only found for SBP. No dose-response effect on BP was observed in diuretics monotherapy group. Conclusions: Pooled evidence of RCTs suggests a dose-response relationship between sodium reduction and BP in treated hypertensives, which is impacted by class of antihypertensive medications.

Multiple Sclerosis and Sodium Toxicity: Controversy and Future Directions for Low-Salt Interventions

Salt intake is associated with multiple sclerosis; however, controversial findings that challenge this association rely primarily on methods that do not measure total sodium storage within the body, such as food surveys and urinary sodium excretion. In contrast, tissue sodium concentrations measured with sodium MRI confirm high sodium levels in multiple sclerosis, suggesting a role for sodium toxicity as a risk factor for the disease. Research on demyelination in the central nervous system has identified myelin phase transitions associated with increased salinity, which cause structural instabilities of myelin sheaths and add further evidence implicating sodium toxicity as a causative factor in multiple sclerosis. Inflammatory and immune responses in multiple sclerosis are also related to high sodium intake. In addition, salt is a potential mediating factor associating multiple sclerosis with comorbidities, including systemic lupus erythematosus, rheumatic arthritis, inflammatory bowel disease, and cardiovascular disease. Current confusion exists over classifying dietary sodium intake levels as low, normal, and high, and questions remain over levels of sodium restriction necessary for disease prevention. To reduce multiple sclerosis symptoms and prevent disease progression in patients, future research should investigate low-salt interventions with levels of sodium intake associated with ancestral hunter-gatherer tribes.

Levels of dietary sodium intake: diverging associations with arterial stiffness and atheromatosis

BackgroundRecent epidemiological evidence suggests a J-shaped, rather than the classical linear, association between dietary sodium (Na) intake and cardiovascular (CV) disease. Numerous animal studies have shown the acceleration of atheromatosis in a low-salt diet but data in humans are scarce. Our aim was to test the hypothesis that in a cohort of patients who are CV-free, yet at increased CV risk, moderate Na intake is associated with lower prevalence of atheromatosis and arterial stiffening than those at very low Na intake. MethodsTwo 24-h dietary recalls were conducted to estimate Na intake. Atheromatosis (carotid and femoral plaques) was assessed by B-mode ultrasonography and arterial stiffness through tonometry (carotid-to-femoral pulse wave velocity, cf-PWV). ResultsIn 901 individuals (age: 52.4 ± 13.8 years, 45.2% males), only females at 3rd and 4th quartile of total Na intake (derived from food and discretionary salt) had significantly lower probability to present femoral plaques than those at 1st quartile (751.0 ± 215.5 mg/day), even in the full-adjusted model [0.462(0.229-0.935) and p = 0.032 3rd quartile; 0.274(0.118-0.638) and p = 0.003 4th quartile]. On the contrary, male and female individuals at 3rd quartile had significantly higher probability to present arterial stiffness (PWV >10 m/s) than those at 1st quartile [1.991(1.047-3.785) and p = 0.036]. ConclusionsOverall, the present data suggest that very low Na intake is associated with: a) accelerated atheromatosis, verifying findings from animal models, and providing a possible explanation of the modern epidemiology and b) lower arterial stiffness, which is in line with previous human findings, therefore suggesting a diverging effect of Na in the two major arterial pathologies.

P4540Obesity in patients with heart failure and without diabetes mellitus is associated with longer event-free survival only among those with high dietary sodium intake

Abstract Background Obesity is paradoxically associated with better short- and long-term outcomes in patients with heart failure (HF) and without diabetes mellitus (DM). While excessive dietary sodium intake is common among obese persons, its impact on the association between obesity and outcomes has not been considered. Aim To determine whether dietary sodium intake levels would affect the association between obesity and better outcomes in patients with HF and without DM. Method A sample of 129 patients (age 60±12.4 years; 30% female) provided a single 24-hour urine collection sample to estimate dietary sodium intake. Patients were divided into 4 groups based on body mass index (BMI) and the sodium intake recommendation for HF of 3g/day (obese with high sodium intake [n=41; 32%], obese with low sodium intake [n=16; 12%], non-obese with high sodium intake [n=35; 27%], and non-obese with low sodium intake [n=37; 29%]). Patients were followed-up during an average period of 395 days to determine time to first event of all-cause hospitalization or death. Cox regression was used to determine the association between obesity and outcomes in the context of sodium intake after controlling for age, gender, NYHA class (I II vs. III IV) and LVEF. Results There were 41 patients (31.8%) who had an event of all-cause hospitalization or death. Obese patients with high sodium intake had 61% lower risk for events than those non-obese with low dietary sodium intake (figure). There were no differences in the event-free survival among other groups. Conclusion These data suggest that dietary sodium intake may be particularly important for obese patients with HF and without DM.

The contribution of skin glycosaminoglycans to the regulation of sodium homeostasis in rats.

The glycosaminoglycan (GAG) molecules are a group of high molecular weight, negatively charged polysaccharides present abundantly in the mammalian organism. By their virtue of ion and water binding capacity, they may affect the redistribution of body fluids and ultimately the blood pressure. Data from the literature suggests that the mitogens Vascular Endothelial Growth Factor (VEGF)-A and VEGF-C are able to regulate the amount and charge density of GAGs and their detachment from the cell surface. Based on these findings we investigated the relationship between the level of dietary sodium intake, the expression levels of VEGF-A and VEGF-C, and the amount of the skin GAGs hyaluronic acid and chondroitin sulfate in an in vivo rat model. Significant correlation between dietary sodium intake, skin sodium levels and GAG content was found. We confirmed the GAG synthesizing role of VEGF-C but failed to prove that GAGs are degraded by VEGF-A. No significant difference in blood pressure was registered between the different dietary groups. A quotient calculated form the ion and water content of the skin tissue samples suggests that - in contrast to previous findings - the osmotically inactive ions and bound water fractions are proportional.

Investigating the Relationship between Dietary Sodium Intake and Severity Levels of Fluid Overload Symptoms in Patients with Heart Failure

<p><strong><em>Aim: </em></strong><em>This study aimed to investigate dietary sodium intake levels and to explore the relationship between those levels and the severity of fluid overload symptoms.</em></p><p><strong><em>Background: </em></strong><em>The management of dietary sodium is an important nursing intervention in the care of patients with heart failure stemming from fluid overload. Recommendations for the intake of dietary sodium among heart failure patients were discussed. If a heart failure patient’s dietary sodium intake habits are understood, then the relationship between this intake and fluid overload can be elucidated. This knowledge would be beneficial for nursing intervention in cases of heart failure.</em></p><p><strong><em>Methods:</em></strong><em> A total of 98 patients selected from cardiology wards who had a diagnosis of heart failure were enrolled in this study. Their dietary sodium intake level was estimated from a 24-hour urinary sodium excretion analysis. The severity of fluid overload symptoms was assessed using the fluid volume overload symptoms scale. </em></p><p><strong><em>Results:</em></strong><em> This study showed that the mean dietary sodium intake for patients with heart failure was 2.49 g/day and that this intake had no correlation with the severity levels of fluid overload symptoms. </em></p><p><strong><em>Conclusions: </em></strong><em>Using the patients’ own perceptions of the severity of fluid overload symptoms as a reference, adopting more relaxed sodium dietary intake restrictions may lead patients to have better food consumption habits.</em></p>

144 - Prospective, Randomised and Blinded Clinical Study Testing Two Levels of Dietary Sodium Intake in Patients with Acute Decompensated Heart Failure

144 - Prospective, Randomised and Blinded Clinical Study Testing Two Levels of Dietary Sodium Intake in Patients with Acute Decompensated Heart Failure

Design of a randomized controlled clinical trial assessing dietary sodium restriction and hemodialysis-related symptom profiles.

AimIn hemodialysis patients, the need to have intercurrent sodium and water intake removed by ultrafiltration increases disease burden through the symptoms and signs that occur during hemodialysis (HD). This added burden may be mitigated by reduction of dietary sodium intake. The National Kidney Foundation (NKF) recommends 2400 mg of dietary sodium daily for patients on HD, and the American Heart Association (AHA) suggests 1500 mg, evidence is lacking, however, to support these recommendations in HD. Moreover, little is known about the relationship of specific levels of dietary sodium intake and the severity of symptoms and signs during ultrafiltration. Our goal will be to determine the effects of carefully-monitored levels of sodium-intake as set forth by the NKF and AHA on symptoms and signs in patients undergoing (HD).MethodsWe designed a three-group (2400 mg, 1500 mg, unrestricted), double blinded randomized controlled trial with a sample of 42 HD participants to determine whether 1. Symptom profiles and interdialytic weight gains vary among three sodium intake groups; 2. The effect of HD-specific variables on the symptom profiles among the three groups and 3. Whether total body water extracellular volume and intracellular volume measured with bioimpedance varies across the three groups. We will also examine the feasibility of recruitment, enrollment, and retention of participants for the five-day inpatient stay.ConclusionCurbing dietary sodium intake may lead to improvement in intradialytic symptom amelioration and potential for better long-term outcomes. Generating empirical support will be critical to ascertain, and espouse, the appropriate level of sodium intake for patients receiving HD.

Effects of dietary sodium and the DASH diet on the occurrence of headaches: results from randomised multicentre DASH-Sodium clinical trial

ObjectivesHeadaches are a common medical problem, yet few studies, particularly trials, have evaluated therapies that might prevent or control headaches. We, thus, investigated the effects on the occurrence of headaches...

Abstract 425: High Sodium Excretion is not Associated with Reduced Vasodilation in Healthy African American Adults

Background: High dietary sodium (Na) intake has been shown to be related to the development of endothelial dysfunction and hypertension. Urinary sodium excretion in people with normal renal function can indirectly reflect the level of dietary sodium intake. The purpose of the study was to test whether high urine Na excretion was independent from other risk factors and related to the compromised endothelial-dependent (fiow-mediated dilation [FMD]) and/or endothelium-independent (nitroglycerin-induced dilation [NMD]) in normotensive African Americans. Normotensives were studied in order to eliminate the influence of hypertension. METHODS: Urine was collected for 24 hr in 30 subjects aged 41-63 yrs with normal blood pressure (125.7 ± 9.7/81 ± 7.1 mmHg). 16 subjects had Na excretion <150 mmol (99.6 ± 24.8 mmol) and were classified as the Normal Na excretion group and 14 subjects had Na excretion ≥150 mmol/g (186.5 ± 27.1 mmol) and were classified as the High Na excretion group. FMD was measured after 5-min cuff occlusion and NMD was measured after application of 0.8 mg nitroglycerin using Doppler ultrasound. The maximum FMD- and NMD-diameters and FMD/NMD ratio were calculated. Results: There were no differences in other dietary factors, age, body mass index, blood pressure, or physical activity levels between the groups. Plasma concentrations of cholesterol, glucose, antioxidant status and inflammatory markers did not differ between groups. FMD (Normal: 7.4 ± 2.9% vs. High: 9.5 ± 3.6%; p=0.09) and NMD (Normal: 17.9 ± 6.3% vs. High: 27.8 ± 18.1%; p=0.07) and true peak FMD/NMD ratio (Normal: 0.45 ± 0.22 vs. High: 0.38 ± 0.11; p=0.26) were not different between groups. No significant correlations were found between 24hr Na excretion and FMD (r=0.332; p=0.073), NMD (r=0.356; p=0.053) or FMD/NMD ratio(r=0.112; p=0.554) in the entire study group. Conclusion: High Na excretion was not associated with reduced endothelial responsiveness in healthy African Americans with normal blood pressure. These results suggest that high Na intake may not be predictive of endothelial dysfunction in putatively healthy populations.

A 4-Day Sodium-Controlled Diet Reduces Variability of Overnight Sodium Excretion in Free-Living Normotensive Adolescents

The present analysis examined changes in the variability of overnight sodium excretion in 84 free-living adolescents (ages 15 to 19 years) on a 4-day sodium-controlled diet in which foods provided were selected by adolescents from an extensive list of menu items. The only selection criterion imposed was that foods selected for each day contain 4,000±200 mg sodium. Adolescents collected overnight urine samples. Repeated measures analysis of variance tested the effect of diet day on overnight sodium excretion, overnight urinary sodium concentration, and overnight urinary volume. Variance ratio test evaluated changes in overnight sodium excretion variance across days. Day 4 overnight sodium excretion was statistically lower than days 1 to 3 (1.84 vs 6.54, 5.94, and 5.52 mEq/h [1.84 vs 6.54, 5.94, and 5.52 mmol/h]). Day 4 overnight urinary sodium concentration was lower than days 1 to 3 (32.16 vs 119.64, 109.61, and 111.32 mEq/L [32.16 vs 119.64, 109.61, and 111.32 mmol/L]). The variance of overnight sodium excretion from day 1 to day 4 was reduced 10-fold from 20.1 mEq/h (20.1 mmol/h) to 1.90 mEq/h (1.90 mmol/h). Daily overnight urine volumes remained constant, averaging 451.7 mL/day. The dietary protocol successfully reduced the variability of sodium intake as estimated by overnight sodium excretion in free-living adolescents. The protocol could be expanded to include baseline values, additional days of sodium control, and varying levels of dietary sodium intake.

The autonomic nervous system and pressure-natriuresis in cardiovascular-renal interactions in response to salt.

The maintenance of cardiovascular homeostasis represents a balance of activities between of the heart, vascular system and the kidneys in the control of extracellular fluid volume and ultimately blood pressure. Any disturbance in the function of these organs can lead to hypertension and heart failure. Interaction between the cardiovascular and renal systems is exerted dynamically by the autonomic nervous system and humoral factors which together determine the slope of the pressure-natriuresis relationship. This allows the body to ensure that dietary sodium intake can be excreted efficiently without causing major changes in blood pressure. Autonomic control of the kidney is exerted via the renal sympathetic nerves modulating renin release, sodium reabsorption and renal haemodynamics. Epidemiological studies have suggested a weak relationship between the level of dietary sodium intake and the development of hypertension, the underlying mechanisms are uncertain. It is evident from experimental studies that an elevation in dietary sodium intake during the growing phase heightens neural control of blood pressure and the kidney partly due to an enhanced role of the brain renin-angiotensin system. The relationship between dietary sodium and the autonomic regulation of blood pressure and the kidney is increasingly recognised as important but is only poorly understood.

Using Angiotensin Converting Enzyme Inhibitors in African-American Hypertensives: A New Approach to Treating Hypertension and Preventing Target-Organ Damage

Angiotensin converting enzyme (ACE) inhibitors have been avoided as an initial therapeutic option in the treatment of hypertension in African-Americans. A major reason for this has been the widespread perception of clinicians that these agents have poor blood pressure (BP) lowering efficacy in this population. Remarkably uniform and pervasive interpretations of clinical trial data have formed the basis of this clinical perception and can be summarised as follows: (1) there has been a lesser BP lowering effect of ACE inhibitors in African-Americans compared to whites, particularly at low doses; and (2) short-acting ACE inhibitors like captopril prescribed at the midpoint of its maximal total daily dose lower BP less effectively than higher doses of calcium antagonists in African-Americans. A reinterpretation of published data from these same clinical trials suggests that: (1) the majority of African-Americans have meaningful BP responses to ACE inhibitors, albeit at a higher average dose than in whites; and (2) high levels of dietary sodium intake appear to explain a significant portion of the racial differences in BP response at the lower doses of ACE inhibitors. Thus, ACE inhibitors can effectively lower BP in African-Americans. These data suggest that the clinician should not avoid these agents in African-Americans because of a presumed lack of BP lowering efficacy. Rather, we should recognise the importance of adequate drug dosing and modest reductions in dietary sodium intake in augmenting the BP lowering effect of ACE inhibitors in hypertensive African-Americans.

Using Angiotensin Converting Enzyme Inhibitors in African-American Hypertensives: A New Approach to Treating Hypertension and Preventing Target-Organ Damage

SummaryAngiotensin converting enzyme (ACE) inhibitors have been avoided as an initial therapeutic option in the treatment of hypertension in African-Americans. A major reason for this has been the widespread perception of clinicians that these agents have poor blood pressure (BP) lowering efficacy in this population. Remarkably uniform and pervasive interpretations of clinical trial data have formed the basis of this clinical perception and can be summarised as follows: (1) there has been a lesser BP lowering effect of ACE inhibitors in African-Americans compared to whites, particularly at low doses; and (2) short-acting ACE inhibitors like captopril prescribed at the midpoint of its maximal total daily dose lower BP less effectively than higher doses of calcium antagonists in African-Americans. A reinterpretation of published data from these same clinical trials suggests that: (1) the majority of African-Americans have meaningful BP responses to ACE inhibitors, albeit at a higher average dose than in whites; and (2) high levels of dietary sodium intake appear to explain a significant portion of the racial differences in BP response at the lower doses of ACE inhibitors. Thus, ACE inhibitors can effectively lower BP in African-Americans. These data suggest that the clinician should not avoid these agents in African-Americans because of a presumed lack of BP lowering efficacy. Rather, we should recognise the importance of adequate drug dosing and modest reductions in dietary sodium intake in augmenting the BP lowering effect of ACE inhibitors in hypertensive African-Americans.

Twenty-four-hour blood pressure profiles in normotensive sons of hypertensive parents.

We investigated whether blood pressures are higher in normotensive offspring of hypertensive parents than in normotensive offspring of normotensive parents outside the physician's office and, if so, whether these higher blood pressures are dependent on the level of dietary sodium intake. We compared 24-hour ambulatory blood pressure profiles between 11 normotensive sons of two hypertensive parents and 11 normotensive sons of two normotensive parents; profiles were recorded after 1 week of a low sodium diet (10 meq/day) and after 1 week of a high sodium diet (200 meq/day). The sons of hypertensive parents were on average 6 years older than the sons of normotensive parents (47 +/- 5 [SD] versus 41 +/- 4 years, p < 0.05). The shift from low to high sodium diet did not significantly change the magnitude of differences in office or ambulatory blood pressures between the groups (i.e., no group-by-diet interaction); thus, we assessed group effects by contrasting blood pressure means for each group pooled across diets. Age-adjusted office blood pressure was higher in sons of hypertensive parents than in sons of normotensive parents (116 +/- 7/80 +/- 6 versus 111 +/- 7/75 +/- 6 mm Hg; p = 0.020 for systolic and p = 0.003 for diastolic blood pressure).(ABSTRACT TRUNCATED AT 250 WORDS)

Left Ventricular Hypertrophy and Pressure Generating Capacity in Aging Genetically Hypertensive Rats

Alterations in the relationship between the degree of left ventricular hypertrophy and the maximum pressure generating capacity were assessed in two models of genetic hypertension in rats. Both the spontaneously hypertensive rat (SHR) and the Dahl salt-sensitive (DS) rat developed systemic hypertension and progressive increases in left ventricular mass. In the DS rat, the magnitude of the hypertension and ventricular hypertrophy produced was in direct relation to the level of dietary sodium intake. At 6 months of age, the pressure generating capacity of all hypertensive rats was directly related to the left ventricular weight/body weight ratio. With the moderate level of hypertrophy observed in the 12-month-old SHRs and DS rats on a low salt diet, the correlation between left ventricular weight and augmented pressure generating capacity during isovolumic contractions was maintained. With the more severe degrees of left ventricular hypertrophy observed in 18- and 24-month-old SHRs and 12-month-old DS rats on a moderate salt diet, the further addition of ventricular mass was no longer associated with a proportional augmentation in maximal pressure development. These studies suggest that in genetic hypertension in rats, both the magnitude and duration of the hypertension are important determinants of the degree of hypertrophy and the functional status of the ventricle.

The Utility of Overnight Urine Collections in Assessing Compliance With a Low Sodium Intake Diet

To develop methods of estimating sodium intake in free-living persons, we gave normal volunteers mean sodium intakes of 65, 110, and 200 mEq/day. The intake was randomly varied about each mean by an SD of 12.5% daily. Twenty-four-hour and night urinary sodium excretion were measured. Night urinary sodium excretion was also estimated by means of inexpensive quantitative and qualitative chloride titrator strips. The latter required no timed urine collection. A total of three 24-hour urine collections were necessary to differentiate the regimens with 95% accuracy. Three night urinary sodium excretory estimates by the quantitative chloride titrator provided 79% accuracy in identifying the level of dietary sodium intake. By applying the qualitative chloride titrator every other day, the dietary regimens could be differentiated with 95% accuracy. These techniques were not only useful in estimating sodium intake, but also provided a simple means of documenting compliance to sodium restriction. Patients should have no difficulty in applying these methods themselves in a home setting.

Autonomic blockade and the Valsalva maneuver in patients on maintenance hemodialysis: A hemodynamic study

Hemodynamic studies were performed at two levels of dietary sodium intake (10 mmoles/day and 100 mmoles/day for 14 days) in a group of patients (with retained kidneys) on chronic hemodialysis. Plasma renin activity and aldosterone, plasma, and extracellular fluid (ECF) volumes were measured while the patient were at rest. Cardiac output, mean intraarterial pressure, and the calculated total peripheral resistance index were recorded while the patients were at rest and during acute "total" autonomic blockade. On the sodium diet of 10 mmoles/day, normotensive and hypertensive patients had similarly low total blood volumes, low-normal ECF volumes, and similar levels of plasma renin and aldosterone. The resting cardiac output was increased in both groups, but the total peripheral resistance was increased only in the patients with hypertension, in whom peripheral resistance was inappropriately high for the degree of anemia. Six hypertensive patients were studied on both diets. The resting mean arterial pressure was greater on the sodium diet of 100 mmoles/day than on the 10 mmoles/day diet, accompanied by increased in plasma volume, extracellular fluid volume, and cardiac output, but no change in peripheral resistance. During autonomic blockade on either diet, there was a marked fall in blood pressure in the patients with hypertension. This was mainly due to a fall in peripheral resistance which reached levels similar to those seen in the normotensive patients whose resistance was unaltered by blockade. Autonomic factors appear to contribute to the elevated peripheral resistance of hypertensive dialysis patients. In these patients, the effect of a high sodium diet, at least over the time-scale studied here, is to increase blood pressure and cardiac output, without the change in peripheral resistance expected from autoregulation.

Effect of dietary sodium intake on the intrarenal distribution of nephron glomerular filtration rates in the rat.

Redistribution of single nephron glomerular filtration rate (SNGFR) between superficial (S) and juxtamedullary (JM) nephrons is thought to participate in the renal adaptation to different levels of dietary sodium intake. This possibility was examined using the Hanssen technique which measures SNGFR as the 14 C-ferrocyanide content of microdissected nephrons factored by the mean plasma concentration following a 12-second infusion. Rats from the same litter were placed on a low-sodium (0.8 mEq/day) or a high-sodium (9 mEq/day) diet. The distribution of SNGFR was measured as the S/JM (mean of S nephrons/mean of JM nephrons) SNGFR ratio. In spite of an eightfold change in sodium excretion, there was no significant change in the S/JM SNGFR ratio (low sodium - high sodium: -0.0033 ± 0.048 [ SE ], P &gt; 0.9). Seven rats that were not littermates were maintained on a standard diet but drank saline (13 mEq sodium/day); carotid and ureteral catheterization and the duration of the diet (3-14 weeks) had no effect on the S/JM SNGFR ratio ( P &gt; 0.1), which was similar to that of nine rats maintained on a standard diet with water for drinking (3 mEq sodium/day). The value of the S/JM SNGFR ratios were 0.77 and 0.83, respectively. These variations in dietary sodium intake appeared to have no detectable effect on the intrarenal SNGFR distribution.